Abstract T P148: Lactate Dehydrogenase Levels are Associated with Acute Ischemic Stroke in Ventricular Assist Device Patients
Background: Patients with Ventricular Assist Devices (VADs) have an increased thromboembolic (TE) risk including a higher risk of acute ischemic stroke (AIS). To mitigate this risk patients are placed on a combination of aspirin, clopidogrel and warfarin with a goal INR of 2-3. VAD patients are at higher risk for hemolysis, which contributes to the risk for TE and AIS. We hypothesize that Lactate Dehydrogenase (LDH) elevation, a marker of hemolysis, is associated with an increased risk of AIS.
Methods: Patients (n=98) receiving a continuous flow VAD at the University of Alabama at Birmingham between 2008 and 2012 were included in this analysis. The association of LDH levels (collected pre-VAD, VAD date, 14 days, 1 month, 3 months, 6 months, 9 months and 12 months after VAD) with AIS was evaluated using time-to-event-analysis adjusting for comorbid conditions, age at implant and antithrombotic therapy.
Results: The median age at implant was 53 (20-76) with 78% patients male, 64% white and 59% serving as a bridge to transplant. The incidence of AIS was 13 events/100 patient years (95% CI 6.85-22.6). No patients received IV t-PA or intraarterial therapy. Patients with elevated LDH (>500) at VAD implant (Figure) were at greater risk for AIS with the association becoming stronger after adjustment (Hazard Ratio (HR) 31.1, 95% CI 0.61-1577, p=0.0863). Elevated LDH at 30-days post VAD implant was associated with a higher risk of AIS, even after adjustment (HR 12.3, 95% CI 1.12-134.9, p=0.0403).
Conclusion: AIS is common among VAD patients despite their antithrombotic regimen. Early elevation of LDH is associated with increased risk of AIS. However, even elevation of LDH on the day of VAD implant appears to be associated with increased AIS risk, indicating non-VAD related LDH elevation may identify a high risk subgroup. Since these patients have contraindications to the standard AIS treatments, identifying predictors, such as LDH, of AIS and preventing AIS are of interest.
Author Disclosures: A.K. Boehme: None. C. Dillon: None. G. McGwin: None. S.V. Pamboukian: None. N.A. Limdi: None.
This research has received full or partial funding support from the American Heart Association, Greater Southeast Affiliate – Alabama, Florida, Georgia, Louisiana, Mississippi, Puerto Rico, Tennessee, U.S. Virgin Islands.
- © 2014 by American Heart Association, Inc.